Differential gene expression profiles in the hippocampus of senescence-accelerated mouse

Cheng, Xiaorui; Zhou, Wenxia; Zhang, Yongxiang; Dong, Zhou; Yang, Ruifu; Chen, Lingfeng

doi:10.1016/j.neurobiolaging.2006.02.004

Cited by 36 publications

(36 citation statements)

References 49 publications

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“…Increase in NQO1 Protein Level Observed in Aged Brain Correlates with STUB1 Decrease-It has been suggested that the STUB1 level is down-regulated with aging (33). Indeed, when examining STUB1 protein levels in the brain of mice of different ages (1, 12, and 36 weeks old) a decrease in STUB1 protein levels was observed with aging whereas the level of its interacting proteins Hsc70 remained unchanged (Fig.…”

Section: Volume 286 • Number 11 • March 18 2011mentioning

confidence: 85%

E3 Ligase STUB1/CHIP Regulates NAD(P)H:Quinone Oxidoreductase 1 (NQO1) Accumulation in Aged Brain, a Process Impaired in Certain Alzheimer Disease Patients

Tsvetkov

Adamovich

Elliott

et al. 2011

Journal of Biological Chemistry

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NAD(P)H:quinone oxidoreductase 1 (NQO1) is a flavoenzyme that is important in maintaining the cellular redox state and regulating protein degradation. The NQO1 polymorphism C609T has been associated with increased susceptibility to various age-related pathologies. We show here that NQO1 protein level is regulated by the E3 ligase STUB1/CHIP (C terminus of Hsc70-interacting protein). NQO1 binds STUB1 via the Hsc70-interacting domain (tetratricopeptide repeat domain) and undergoes ubiquitination and degradation. We demonstrate here that the product of the C609T polymorphism (P187S) is a stronger STUB1 interactor with increased susceptibility to ubiquitination by the E3 ligase STUB1. Furthermore, age-dependent decrease of STUB1 correlates with increased NQO1 accumulation. Remarkably, examination of hippocampi from Alzheimer disease patients revealed that in half of the cases examined the NQO1 protein level was undetectable due to C609T polymorphism, suggesting that the age-dependent accumulation of NQO1 is impaired in certain Alzheimer disease patients.

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Section: Volume 286 • Number 11 • March 18 2011mentioning

confidence: 85%

E3 Ligase STUB1/CHIP Regulates NAD(P)H:Quinone Oxidoreductase 1 (NQO1) Accumulation in Aged Brain, a Process Impaired in Certain Alzheimer Disease Patients

Tsvetkov

Adamovich

Elliott

et al. 2011

Journal of Biological Chemistry

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“…A lot of studies have been carried out to examine the changes in expression of the proteins [40,54,65,67,70,74,78,[92][93][94][95] and genes [96][97][98][99][100][101][102] in the brains of SAMP8 mice, helping our understanding of the etiopathogenesis of neurodegenerative disorders in the SAMP8 mice.…”

Section: Protein and Gene Expression Studiesmentioning

confidence: 99%

Senescence-Accelerated Mouse (SAM) with Special References to Neurodegeneration Models, SAMP8 and SAMP10 Mice

Takeda¹

2009

Neurochem Res

215

188

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The SAM strains, a group of related inbred strains consisting of senescence-prone inbred strains (SAMP) and senescence-resistant inbred strains (SAMR), have been successfully developed by selective inbreeding of the AKR/J strain of mice donated by the Jackson laboratory in 1968. The characteristic feature of aging common to the SAMP and SAMR is accelerated senescence and normal aging, respectively. Furthermore, SAMP and SAMR strains of mice manifest various pathobiological phenotypes spontaneously. Among SAMP strains, SAMP8 and SAMP10 mice show age-related behavioral deterioration such as deficits in learning and memory, emotional disorders (reduced anxiety-like behavior and depressive behavior) and altered circadian rhythm associated with certain pathological, biochemical and pharmacological changes. Here, the previous and recent literature on SAM mice are reviewed with an emphasis on SAMP8 and SAMP10 mice. A spontaneous model like SAM with distinct advantages over the gene-modified model is hoped by investigators to be used more widely as a biogerontological resource to explore the etiopathogenesis of accelerated senescence and neurodegenerative disorders.

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“…Cheng and coworkers [41] used subtractive cDNA libraries containing 3136 cDNA to show that the profiles of gene expression in the hippocampus of 12-monthold SAMP8 and SAMR1 were significantly different and may play important roles in the age-related learning and memory deficit in SAMP8. In this study, of all 91 differentially expressed genes, 50 were upregulated and 41 were downregulated in the hippocampus of 12-month-old male SAMP8 compared with age-matched SAMR1.…”

Section: Genomic Approach: the Unknownmentioning

confidence: 99%

Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model

Pallàs

2012

ISRN Cell Biology

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The causes of aging remain unknown, but they are probably intimately linked to a multifactorial process that affects cell networks to varying degrees. Although a growing number of aging and Alzheimer's disease (AD) animal models are available, a more comprehensive and physiological mouse model is required. In this context, the senescence-accelerated mouse prone 8 (SAMP8) has a number of advantages, since its rapid physiological senescence means that it has about half the normal lifespan of a rodent. In addition, according to data gathered over the last five years, some of its behavioral traits and histopathology resemble AD human dementia. SAMP8 has remarkable pathological similarities to AD and may prove to be an excellent model for acquiring more in-depth knowledge of the age-related neurodegenerative processes behind brain senescence and AD in particular. We review these facts and particularly the data on parameters related to neurodegeneration. SAMP8 also shows signs of aging in the immune, vascular, and metabolic systems, among others.

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Differential gene expression profiles in the hippocampus of senescence-accelerated mouse

Cited by 36 publications

References 49 publications

E3 Ligase STUB1/CHIP Regulates NAD(P)H:Quinone Oxidoreductase 1 (NQO1) Accumulation in Aged Brain, a Process Impaired in Certain Alzheimer Disease Patients

E3 Ligase STUB1/CHIP Regulates NAD(P)H:Quinone Oxidoreductase 1 (NQO1) Accumulation in Aged Brain, a Process Impaired in Certain Alzheimer Disease Patients

Senescence-Accelerated Mouse (SAM) with Special References to Neurodegeneration Models, SAMP8 and SAMP10 Mice

Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model

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